Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
Texto Completo: | https://doi.org/10.1038/s41598-017-05687-1 |
Resumo: | We would like to thank Prof. Ira Tabas (Columbia University, New York, NY, USA) for providing the L929 cell line, Prof. Herbert Virgin (Washington University, St. Louis, MO, USA) for providing p62-KO mice legs, Dr. H. Girao (CNC. IBILI, Univ. of Coimbra) for the E1-inhibitor and T. Pereira for technical assistance with microscopy. This work was supported by the Foundation for Science and Technology of the Portuguese Ministry of Science and Higher Education [HMSP-ICT/0024/2010, co-founded by the European Union (FEDER - Fundo Europeu de Desenvolvimento Regional) through COMPETE - Programa Operacional Factores de Competitividade and QREN - Quadro de Referencia Estrategico], iNOVA4Health - UID/Multi/04462/2013, a program financially supported by FCT through national funds and co-funded by FEDER under the PT2020 Partnership Agreement and FCT to OVV. PhD fellowships SFRH/BD/62197/2009, SFRH/BD/90258/2012 and SFRH/BD/51877/2012 and SFRH/BD/52293/2013. PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010, European Community 7th Framework Grant ERC-2011-AdG 294709-DAMAGECONTROL to MPS. Editor |
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Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosisWe would like to thank Prof. Ira Tabas (Columbia University, New York, NY, USA) for providing the L929 cell line, Prof. Herbert Virgin (Washington University, St. Louis, MO, USA) for providing p62-KO mice legs, Dr. H. Girao (CNC. IBILI, Univ. of Coimbra) for the E1-inhibitor and T. Pereira for technical assistance with microscopy. This work was supported by the Foundation for Science and Technology of the Portuguese Ministry of Science and Higher Education [HMSP-ICT/0024/2010, co-founded by the European Union (FEDER - Fundo Europeu de Desenvolvimento Regional) through COMPETE - Programa Operacional Factores de Competitividade and QREN - Quadro de Referencia Estrategico], iNOVA4Health - UID/Multi/04462/2013, a program financially supported by FCT through national funds and co-funded by FEDER under the PT2020 Partnership Agreement and FCT to OVV. PhD fellowships SFRH/BD/62197/2009, SFRH/BD/90258/2012 and SFRH/BD/51877/2012 and SFRH/BD/52293/2013. PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010, European Community 7th Framework Grant ERC-2011-AdG 294709-DAMAGECONTROL to MPS. EditorErythrophagocytosis, the phagocytic removal of damaged red blood cells (RBC), and subsequent phagolysosome biogenesis are important processes in iron/heme metabolism and homeostasis. Phagolysosome biogenesis implies the interaction of nascent phagosomes with endocytic compartments and also autophagy effectors. Here, we report that besides recruitment of microtubule-associated protein-1-light chain 3 (LC3), additional autophagy machinery such as sequestosome 1 (p62) is also acquired by single-membrane phagosomes at very early stages of the phagocytic process and that its acquisition is very important to the outcome of the process. In bone marrow-derived macrophages (BMDM) silenced for p62, RBC degradation is inhibited. P62, is also required for nuclear translocation and activation of the transcription factor Nuclear factor E2-related Factor 2 (NRF2) during erythrophagocytosis. Deletion of the Nrf2 allele reduces p62 expression and compromises RBC degradation. In conclusion, we reveal that erythrophagocytosis relies on an interplay between p62 and NRF2, potentially acting as protective mechanism to maintain reactive oxygen species at basal levels and preserve macrophage homeostasis. © 2017 The Author(s).Centro de Estudos de Doenças Crónicas (CEDOC)NOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)RUNSantarino, I.B.Viegas, M.S.Domingues, N.S.Ribeiro, A.M.Soares, M.P.Vieira, O.V.2017-10-26T22:02:48Z2017-07-192017-07-19T00:00:00Zinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article16application/pdfhttps://doi.org/10.1038/s41598-017-05687-1eng2045-2322PURE: 3163755https://www.scopus.com/inward/record.uri?eid=2-s2.0-85025474729&doi=10.1038%2fs41598-017-05687-1&partnerID=40&md5=823d512cab68e52a6b235c2be8dd32e8https://doi.org/10.1038/s41598-017-05687-1info:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2024-05-22T17:28:21Zoai:run.unl.pt:10362/24640Portal AgregadorONGhttps://www.rcaap.pt/oai/openairemluisa.alvim@gmail.comopendoar:71602024-05-22T17:28:21Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse |
dc.title.none.fl_str_mv |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
title |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
spellingShingle |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis Santarino, I.B. |
title_short |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
title_full |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
title_fullStr |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
title_full_unstemmed |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
title_sort |
Involvement of the p62/NRF2 signal transduction pathway on erythrophagocytosis |
author |
Santarino, I.B. |
author_facet |
Santarino, I.B. Viegas, M.S. Domingues, N.S. Ribeiro, A.M. Soares, M.P. Vieira, O.V. |
author_role |
author |
author2 |
Viegas, M.S. Domingues, N.S. Ribeiro, A.M. Soares, M.P. Vieira, O.V. |
author2_role |
author author author author author |
dc.contributor.none.fl_str_mv |
Centro de Estudos de Doenças Crónicas (CEDOC) NOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM) RUN |
dc.contributor.author.fl_str_mv |
Santarino, I.B. Viegas, M.S. Domingues, N.S. Ribeiro, A.M. Soares, M.P. Vieira, O.V. |
description |
We would like to thank Prof. Ira Tabas (Columbia University, New York, NY, USA) for providing the L929 cell line, Prof. Herbert Virgin (Washington University, St. Louis, MO, USA) for providing p62-KO mice legs, Dr. H. Girao (CNC. IBILI, Univ. of Coimbra) for the E1-inhibitor and T. Pereira for technical assistance with microscopy. This work was supported by the Foundation for Science and Technology of the Portuguese Ministry of Science and Higher Education [HMSP-ICT/0024/2010, co-founded by the European Union (FEDER - Fundo Europeu de Desenvolvimento Regional) through COMPETE - Programa Operacional Factores de Competitividade and QREN - Quadro de Referencia Estrategico], iNOVA4Health - UID/Multi/04462/2013, a program financially supported by FCT through national funds and co-funded by FEDER under the PT2020 Partnership Agreement and FCT to OVV. PhD fellowships SFRH/BD/62197/2009, SFRH/BD/90258/2012 and SFRH/BD/51877/2012 and SFRH/BD/52293/2013. PTDC/SAU-TOX/116627/2010, HMSP-ICT/0022/2010, European Community 7th Framework Grant ERC-2011-AdG 294709-DAMAGECONTROL to MPS. Editor |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-10-26T22:02:48Z 2017-07-19 2017-07-19T00:00:00Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://doi.org/10.1038/s41598-017-05687-1 |
url |
https://doi.org/10.1038/s41598-017-05687-1 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
2045-2322 PURE: 3163755 https://www.scopus.com/inward/record.uri?eid=2-s2.0-85025474729&doi=10.1038%2fs41598-017-05687-1&partnerID=40&md5=823d512cab68e52a6b235c2be8dd32e8 https://doi.org/10.1038/s41598-017-05687-1 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
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openAccess |
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16 application/pdf |
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Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) |
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Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informação |
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